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[PMID]: 24617837
[Au] Autor:Rubio-Martínez LM; Hendrickson DA; Stetter M; Zuba JR; Marais HJ
[Ad] Address:Department of Companion Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa.
[Ti] Title:Laparoscopic Vasectomy in African Elephants (Loxodonta africana).
[So] Source:Vet Surg;43(5):507-14, 2014 Jul.
[Is] ISSN:1532-950X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To describe a surgical technique for, and outcome after, laparoscopic vasectomy of free-ranging elephants. STUDY DESIGN: Case series. ANIMALS: African elephants (Loxodonta africana; n = 14). METHODS: Male elephants (12-35 years old) were anesthetized with etorphine and supported in a sling in a modified standing position, and positive pressure ventilated with oxygen. Anesthesia was maintained with IV etorphine. Vasectomy was performed under field conditions by bilateral, open-approach, flank laparoscopy with the abdomen insufflated with filtered ambient air. A 4-cm segment of each ductus deferens was excised. Behavior and incision healing were recorded for 8 months postoperatively. RESULTS: Successful bilateral vasectomy (surgical time, 57-125 minutes) was confirmed by histologic examination of excised tissue. Recovery was uneventful without signs of abnormal behavior. Large intestine lacerations (3 elephants; 1 full and 2 partial thickness) were sutured extracorporeally. One elephant found dead at 6 weeks, had no prior abnormal signs. Skin incisions healed without complication. CONCLUSIONS: Laparoscopic vasectomy can be performed in African elephants in their natural environment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/j.1532-950X.2014.12163.x

  2 / 258513 MEDLINE  
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[PMID]: 24831767
[Au] Autor:Hirota JA; Alexis NE; Pui M; Wong S; Fung E; Hansbro P; Knight DA; Sin DD; Carlsten C
[Ad] Address:James Hogg Research Centre, University of British Columbia; Vancouver Coastal Health Research Institute, Vancouver General Hospital, Vancouver, British Columbia, Canada.
[Ti] Title:PM10-stimulated airway epithelial cells activate primary human dendritic cells independent of uric acid: Application of an in vitro model system exposing dendritic cells to airway epithelial cell-conditioned media.
[So] Source:Respirology;19(6):881-90, 2014 Aug.
[Is] ISSN:1440-1843
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:BACKGROUND AND OBJECTIVE: Airway epithelial cells represent the first line of defence against inhaled insults, including air pollution. Air pollution can activate innate immune signalling in airway epithelial cells leading to the production of soluble mediators that can influence downstream inflammatory cells. Our objective was to develop and validate a model of dendritic cell exposure to airway epithelial cell-conditioned media. After establishing the model, we explored how soluble mediators released from airway epithelial cells in response to air pollution influenced the phenotype of dendritic cells. METHODS: Human airway epithelial cells were cultured under control and urban particulate matter (PM10) exposure conditions with or without pharmacological inhibitors of the uric acid pathway. Culture supernatants were collected for conditioned media experiments with peripheral blood mononuclear cell-derived dendritic cells analysed by flow cytometry. RESULTS: Monocytes derived from peripheral blood mononuclear cells cultured in interleukin-4 and granulocyte macrophage colony stimulating factor differentiated into immature dendritic cells that phenotypically differentiated into mature dendritic cells in response to conditioned media from phorbol myristate acetate-activated THP-1 monocytes. Exposure of immature dendritic cells to conditioned media from airway epithelial cells exposed to PM10 resulted in dendritic cell maturation that was independent of uric acid. CONCLUSIONS: We present a conditioned media model useful for interrogating the contribution of soluble mediators produced by airway epithelial cells to dendritic cell phenotype and function. Furthermore, we demonstrate that PM10 exposure induces airway epithelial cell production of soluble mediators that induce maturation of dendritic cells independent of uric acid.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/resp.12316

  3 / 258513 MEDLINE  
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[PMID]: 24874557
[Au] Autor:Mosher BP; Taylor BE; Harris MB
[Ad] Address:University of Alaska Fairbanks, Biology and Wildlife Department, Fairbanks, AK, United States.
[Ti] Title:Intermittent hypercapnia enhances CO2 responsiveness and overcomes serotonergic dysfunction.
[So] Source:Respir Physiol Neurobiol;200:33-9, 2014 Aug 15.
[Is] ISSN:1878-1519
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Serotonergic dysfunction compromises ventilatory chemosensitivity and may enhance vulnerability to pathologies such as the Sudden Infant Death Syndrome (SIDS). We have shown raphé contributions to central chemosensitivity involving serotonin (5-HT)-and γ-aminobutyric acid (GABA)-mediated mechanisms. We tested the hypothesis that mild intermittent hypercapnia (IHc) induces respiratory plasticity, due in part to strengthening of GABA mechanisms. Rat pups were IHc-pretreated (eight consecutive cycles; 5min 5% CO2 - air, 10min air) or constant normocapnia-pretreated as a control, each day for 5 consecutive days beginning at P12. We subsequently assessed CO2 responsiveness using the in situ perfused brainstem preparation. Hypercapnic responses were determined with and without pharmacological manipulation. Results show IHc-pretreatment induces plasticity sufficient for responsiveness despite removal of otherwise critical ketanserin-sensitive mechanisms. Responsiveness following IHc-pretreatment was absent if ketanserin was combined with GABAergic antagonism, indicating that plasticity depends on GABAergic mechanisms. We propose that IHc-induced plasticity could reduce the severity of reflex dysfunctions underlying pathologies such as SIDS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 258513 MEDLINE  
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[PMID]: 24585737
[Au] Autor:Milne-Price S; Miazgowicz KL; Munster VJ
[Ad] Address:Division of Intramural Research, Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
[Ti] Title:The emergence of the Middle East Respiratory Syndrome coronavirus.
[So] Source:Pathog Dis;71(2):119-34, 2014 Jul.
[Is] ISSN:2049-632X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:On September 20, 2012, a Saudi Arabian physician reported the isolation of a novel coronavirus from a patient with pneumonia on ProMED-mail. Within a few days, the same virus was detected in a Qatari patient receiving intensive care in a London hospital, a situation reminiscent of the role air travel played in the spread of severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002. SARS-CoV originated in China's Guangdong Province and affected more than 8000 patients in 26 countries before it was contained 6 months later. Over a year after the emergence of this novel coronavirus - Middle East respiratory syndrome coronavirus (MERS-CoV) - it has caused 178 laboratory-confirmed cases and 76 deaths. The emergence of a second highly pathogenic coronavirus within a decade highlights the importance of a coordinated global response incorporating reservoir surveillance, high-containment capacity with fundamental and applied research programs, and dependable communication pathways to ensure outbreak containment. Here, we review the current state of knowledge on the epidemiology, ecology, molecular biology, clinical features, and intervention strategies of the novel coronavirus, MERS-CoV.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/2049-632X.12166

  5 / 258513 MEDLINE  
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[PMID]: 24844873
[Au] Autor:De Kauwe MG; Medlyn BE; Zaehle S; Walker AP; Dietze MC; Wang YP; Luo Y; Jain AK; El-Masri B; Hickler T; Wårlind D; Weng E; Parton WJ; Thornton PE; Wang S; Prentice IC; Asao S; Smith B; McCarthy HR; Iversen CM; Hanson PJ; Warren JM; Oren R; Norby RJ
[Ad] Address:Department of Biological Sciences, Macquarie University, Sydney, New South Wales, 2109, Australia.
[Ti] Title:Where does the carbon go? A model-data intercomparison of vegetation carbon allocation and turnover processes at two temperate forest free-air CO2 enrichment sites.
[So] Source:New Phytol;203(3):883-99, 2014 Aug.
[Is] ISSN:1469-8137
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Elevated atmospheric CO2 concentration (eCO2 ) has the potential to increase vegetation carbon storage if increased net primary production causes increased long-lived biomass. Model predictions of eCO2 effects on vegetation carbon storage depend on how allocation and turnover processes are represented. We used data from two temperate forest free-air CO2 enrichment (FACE) experiments to evaluate representations of allocation and turnover in 11 ecosystem models. Observed eCO2 effects on allocation were dynamic. Allocation schemes based on functional relationships among biomass fractions that vary with resource availability were best able to capture the general features of the observations. Allocation schemes based on constant fractions or resource limitations performed less well, with some models having unintended outcomes. Few models represent turnover processes mechanistically and there was wide variation in predictions of tissue lifespan. Consequently, models did not perform well at predicting eCO2 effects on vegetation carbon storage. Our recommendations to reduce uncertainty include: use of allocation schemes constrained by biomass fractions; careful testing of allocation schemes; and synthesis of allocation and turnover data in terms of model parameters. Data from intensively studied ecosystem manipulation experiments are invaluable for constraining models and we recommend that such experiments should attempt to fully quantify carbon, water and nutrient budgets.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/nph.12847

  6 / 258513 MEDLINE  
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[PMID]: 25030207
[Au] Autor:Pum D; Sleytr UB
[Ad] Address:Institute of Biophysics, Department of Nanobiotechnology, University of Natural Resources and Life Sciences, Vienna, Muthgasse 11, 1190 Vienna, Austria.
[Ti] Title:Reassembly of S-layer proteins.
[So] Source:Nanotechnology;25(31):312001, 2014 Aug 8.
[Is] ISSN:1361-6528
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Crystalline bacterial cell surface layers (S-layers) represent the outermost cell envelope component in a broad range of bacteria and archaea. They are monomolecular arrays composed of a single protein or glycoprotein species and represent the simplest biological membranes developed during evolution. They are highly porous protein mesh works with unit cell sizes in the range of 3 to 30 nm, and pore sizes of 2 to 8 nm. S-layers are usually 5 to 20 nm thick (in archaea, up to 70 nm). S-layer proteins are one of the most abundant biopolymers on earth. One of their key features, and the focus of this review, is the intrinsic capability of isolated native and recombinant S-layer proteins to form self-assembled mono- or double layers in suspension, at solid supports, the air-water interface, planar lipid films, liposomes, nanocapsules, and nanoparticles. The reassembly is entropy-driven and a fascinating example of matrix assembly following a multistage, non-classical pathway in which the process of S-layer protein folding is directly linked with assembly into extended clusters. Moreover, basic research on the structure, synthesis, genetics, assembly, and function of S-layer proteins laid the foundation for their application in novel approaches in biotechnology, biomimetics, synthetic biology, and nanotechnology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1088/0957-4484/25/31/312001

  7 / 258513 MEDLINE  
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[PMID]: 25045340
[Au] Autor:Kim HP; Yusoff AR; Lee HJ; Lee SJ; Kim HM; Seo GJ; Youn JH; Jang J
[Ad] Address:Department of Information Display and Advanced Display Research Center, Kyung Hee University, Dongdaemun-ku, Seoul 130-171, Republic of Korea....
[Ti] Title:Effect of ZnO:Cs2CO3 on the performance of organic photovoltaics.
[So] Source:Nanoscale Res Lett;9(1):323, 2014.
[Is] ISSN:1931-7573
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We demonstrate a new solution-processed electron transport layer (ETL), zinc oxide doped with cesium carbonate (ZnO:Cs2CO3), for achieving organic photovoltaics (OPVs) with good operational stability at ambient air. An OPV employing the ZnO:Cs2CO3 ETL exhibits a fill factor of 62%, an open circuit voltage of 0.90 V, and a short circuit current density of -6.14 mA/cm(2) along with 3.43% power conversion efficiency. The device demonstrated air stability for a period over 4 weeks. In addition, we also studied the device structure dependence on the performance of organic photovoltaics. Thus, we conclude that ZnO:Cs2CO3 ETL could be employed in a suitable architecture to achieve high-performance OPV.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Da] Date of entry for processing:140721
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1186/1556-276X-9-323

  8 / 258513 MEDLINE  
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[PMID]: 24792231
[Au] Autor:Hegland KW; Okun MS; Troche MS
[Ad] Address:Department of Speech, Language and Hearing Sciences, University of Florida, 336 Dauer Hall, Gainesville, FL, 32611, USA, kwheeler@ufl.edu.
[Ti] Title:Sequential voluntary cough and aspiration or aspiration risk in Parkinson's disease.
[So] Source:Lung;192(4):601-8, 2014 Aug.
[Is] ISSN:1432-1750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Disordered swallowing, or dysphagia, is almost always present to some degree in people with Parkinson's disease (PD), either causing aspiration or greatly increasing the risk for aspiration during swallowing. This likely contributes to aspiration pneumonia, a leading cause of death in this patient population. Effective airway protection is dependent upon multiple behaviors, including cough and swallowing. Single voluntary cough function is disordered in people with PD and dysphagia. However, the appropriate response to aspirate material is more than one cough, or sequential cough. The goal of this study was to examine voluntary sequential coughing in people with PD, with and without dysphagia. METHODS: Forty adults diagnosed with idiopathic PD produced two trials of sequential voluntary cough. The cough airflows were obtained using pneumotachograph and facemask and subsequently digitized and recorded. All participants received a modified barium swallow study as part of their clinical care, and the worst penetration-aspiration score observed was used to determine whether the patient had dysphagia. RESULTS: There were significant differences in the compression phase duration, peak expiratory flow rates, and amount of air expired of the sequential cough produced by participants with and without dysphagia. CONCLUSIONS: The presence of dysphagia in people with PD is associated with disordered cough function. Sequential cough, which is important in removing aspirate material from large- and smaller-diameter airways, is also impaired in people with PD and dysphagia compared with those without dysphagia. There may be common neuroanatomical substrates for cough and swallowing impairment in PD leading to the co-occurrence of these dysfunctions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00408-014-9584-7

  9 / 258513 MEDLINE  
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[PMID]: 24691890
[Au] Autor:Rubini A; Porzionato A; Sarasin G; Zara S; Macchi V; Camporesi E; Bosco G
[Ad] Address:Department of Biomedical Sciences, Section Physiology, University of Padova, Via Marzolo, 3, 35100, Padua, Italy, alessandro.rubini@unipd.it.
[Ti] Title:Hyperbaric Air Exposure at 2.5 ATA Does Not Affect Respiratory Mechanics and Lung Histology in the Rat.
[So] Source:Lung;192(4):609-14, 2014 Aug.
[Is] ISSN:1432-1750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the "ohmic" and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (hyperbarism) lasting 90 min. METHODS: We used the end-inflation occlusion method on anesthetized rats after about 15 min from previous exposure to hyperbarism. The method allows the measurements of respiratory system elastance and of the ohmic and viscoelastic components of airway resistance, which respectively depend on the Newtonian pressure dissipation due to the ohmic airway resistance to airflow and on the viscoelastic pressure dissipation caused by respiratory system tissue stress relaxation. The expressions of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in the lung's tissues were also investigated, together with the histological characteristics of lung tissue. Data were compared with those obtained in control animals and in previously studied animals exposed to hyperoxic hyperbarism. RESULTS: Unlike with hyperoxic hyperbarism, hyperbarism per se did not change significantly the parameters of respiratory mechanics in the control animals (respiratory system elastance and ohmic and viscoelastic resistances were 2.01 ± 0.17 vs. 1.74 ± 0.08 cm H2O/ml, and 0.13 ± 0.02 vs. 0.13 ± 0.03 and 0.425 ± 0.04 vs. 0.33 ± 0.03 cm H2O/ml s(-1) in control vs. experimental animals, respectively, none significantly different), nor did it induce evident effects on lung histology. An increment of both iNOS and eNOS expressions was documented instead (0.50 ± 0.05 vs. 0.75 ± 0.07 and 1.04 ± 0.1 and 1.4 ± 0.15, respectively). CONCLUSION: Our results indicate that, at variance with hyperoxic hyperbarism, the acute exposure to only hyperbarism does not affect either the elastic or the resistive respiratory system properties, or lung histology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00408-014-9576-7

  10 / 258513 MEDLINE  
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[PMID]: 25045361
[Au] Autor:Kim HY; Shin YH; Han MY
[Ad] Address:Department of Pediatrics, Bundang JeSaeng General Hospital, Seongnam, Korea.
[Ti] Title:Determinants of sensitization to allergen in infants and young children.
[So] Source:Korean J Pediatr;57(5):205-10, 2014 May.
[Is] ISSN:1738-1061
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Atopic sensitization is a complex phenomenon that changes dynamically with age throughout childhood; its prevalence increases with age in young children. Additionally, with increasing age, the prevalence of sensitization to inhalant allergens and the prevalence of polysensitization to allergens increase. It is also well established that the development of atopic sensitization is the result of a complex interplay of genetic and environmental factors. However, there is considerable heterogeneity in the literature in terms of the effect of different environmental exposures in young children on the subsequent risk of atopic sensitization and allergic diseases. Previous studies on the relationship, in early life, between pet ownership, sex, exposure to secondhand smoke, exposure to traffic-related air pollution components, and atopic sensitization have yielded different results. Recent studies have highlighted the importance of gene-environment interactions, especially during early childhood, on the risk of subsequent atopic sensitization and allergic diseases. Therefore, pediatricians should consider the genetic and environmental determinants of atopic sensitization in infants and young children when diagnosing and treating patients with allergic diseases. Determining ways in which early exposure to these risk factors in young children may be reduced could be beneficial in preventing the likelihood of developing atopic sensitization.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1407
[Da] Date of entry for processing:140721
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3345/kjp.2014.57.5.205


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